Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multifocal Kaposi's sarcoma in a patient with chronic myeloid leukemia treated with busulfan, a cytostatic and suppressive drug, is reviewed. After five years of treatment, during which temporary remissions occurred, the patient experienced a relapse of leukemia and a considerable immune deficiency. This was expressed by a decrease in the ratio of CD4/CD8 lymphocytes in the peripheral blood. The relation of Kaposi's sarcoma with leukemia, as well as with the state of immunity in this case, does not evoke any doubts. Verification of oncologic treatment brought about a remission of leukemia, an improvement in the patient's immune state, as well as an inhibition of new foci of the Kaposi's sarcoma in the skin in the course of a few months of follow-up evaluation.
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PMID:Kaposi's sarcoma following long-term immunosuppressive therapy: clinical, histologic, and ultrastructural study. 953 54

Mice infected with the LP-BM5 murine leukemia virus (MuLV) develop an immune deficiency syndrome together with an encephalopathy characterized by impairments in spatial learning and memory. These cognitive deficits are evident before the appearance of neuron loss and lymphoid cell invasion of the brain. Nonetheless, a prominent gliosis and a variety of neurochemical changes precede the development of cognitive deficits. The neurochemical abnormalities include significant decreases in striatal Met-enkephalin and substance P (but not somatostatin), increases in concentrations of quinolinic acid and platelet-activating factor, and alterations in brain fyn kinase. At this stage of the infection, some of these neurochemical changes can be reversed by glutamate receptor antagonists, cytokine inhibitors, and anti-retroviral agents. In later stages of the infection, however, the infected mice develop irreversible neuronal loss, invasion of hematopoietic cells, and increased viral burden in the CNS. In addition, motor-neuron dysfunction (hindlimb paralysis, weakness, and ataxia) and seizures are sometimes observed during the late stages of infection. Thus, the LP-BM5 MuLV-infected mouse is a useful model for studying the chronology of neurodegenerative changes, ranging from reversible neuron dysfunction to irreversible neuron loss, that are associated with retrovirus-induced immunodeficiency.
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PMID:The encephalopathy associated with murine acquired immunodeficiency syndrome. 962 8

The aetiology of non-Hodgkin's lymphomas remains a controversial matter, but, recently, evidence has emerged showing that these neoplastic aberrations of the immune system may be due to viruses, at least in some cases. In fact, patients affected by an inherited immune deficiency, and those presenting disease characterized by autoimmune dysfunctions, show an increased risk for the development of non-Hodgkin's lymphomas. Several viruses have been identified as potential aetiologic agents for of non-Hodgkin's lymphomas: one of these is the Epstein-Barr virus, which has been detected in cultures of tumour cells from patients with Burkitt's lymphoma: this virus seems to be involved also in the pathogenesis of some histological variants of Hodgkin's disease. In addition, the human T-cell lymphotrophic virus family members have also been recognized as possible aetiologic agents for several lymphomas, such as cutaneous T-cell lymphomas, T-cell leukaemia and T-cell hairy cell leukaemia. Recently, hepatitis C virus has been recognized as the aetiologic agent of mixed cryoglobulinaemia, which can be considered as a benign lymphoproliferative disorder. Since mixed cryoglobulinaemia can frequently evolve into more aggressive haematological disorders, an increased prevalence of hepatitis C virus infection in non-Hodgkin's lymphomas has been found, especially in low-grade non-Hodgkin's lymphomas. The possible aetiopathogenetic role of hepatitis C virus in non-Hodgkin's lymphomas is discussed on the basis of molecular, clinical and epidemiological considerations.
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PMID:Hepatitis C virus, mixed cryoglobulinaemia and non-Hodgkin's lymphoma. 978 44

Significant strides have been made in our understanding of the biology and treatment of B cell chronic lymphocytic leukemia. Recent studies have defined cytogenetic and molecular lesions that may be responsible for leukemogenesis or disease progression. Molecular analyses of immunoglobulin genes have delineated two or more subgroups of chronic lymphocytic leukemia that may differ in their clinical behavior. Research in the biochemistry of chronic lymphocytic leukemia has provided insight into the noted resistance of leukemia cells to cytotoxic drugs. Investigations into the immunology has revealed mechanisms whereby chronic lymphocytic leukemia cells can contribute to the immune deficiency that commonly develops in patients with this disease. Clinical studies have delineated factors that are helpful in predicting prognosis and have provided data on promising new therapies for patients with this disease, including stem cell transplantation, monoclonal antibodies, and gene therapy.
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PMID:Chronic lymphocytic leukemia. 1040 Mar 75

Bruton's tyrosine kinase (Btk) is required for normal B cell development and signal transduction through cell surface molecules, and its defects lead to X-linked immune deficiency in mice and X-linked agammaglobulinemia in humans. In this report, we will describe the identification and characterization of a molecule, BAM11, which binds to the pleckstrin homology domain of Btk. A sequence homology search revealed that BAM11 has 89% homology, at the amino acid level, to human LTG19/ENL, that was originally identified as one of the fusion partners involved in chromosomal translocations of 11q23, MLL/ALL-1/HRX, in leukemia cells. Deletion mutants demonstrated that the region of BAM11 required for binding to Btk was localized between amino acid residues 240 and 256. Forced expression of a truncated form of BAM11 (amino acids 246-368) inhibited IL-5-induced proliferation by 50%, whereas forced expression of full-length BAM11 in Y16 cells did not affect the IL-5 responsiveness. We have also shown that BAM11 (amino acids 246-368) inhibited the kinase activity of Btk. These results suggest that the binding of BAM11 to Btk plays a regulatory role in the Btk signal transduction pathway. A cell fractionation study and analysis using EGFP-fused Btk protein demonstrated that a proportion of Btk is present within the nucleus.
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PMID:Identification and characterization of a molecule, BAM11, that associates with the pleckstrin homology domain of mouse Btk. 1100 57

To investigate the molecular mechanisms of the variable (diversity) joining (V(D)J) recombination process at an endogenous gene locus, recombination-inducible cell lines were made from both bcl-2-bearing severe combined immune deficiency (scid) homozygous and scid heterozyous (s/ + ) mice by transforming pre-B cells with the temperature-sensitive Abelson murine leukemia virus (ts-Ab-MLV). These transformants can be induced to undergo immunoglobulin light-chain gene rearrangements by incubating them at the non-permissive temperature. In the case of transformed scid cells, a significant amount of hairpin coding ends are accumulated during recombination induction, but few coding joints are generated. After being shifted to the permissive temperature. however, these cells are capable of opening hairpin ends and forming coding joints. Thus, ts-Ab-MLV transformed scid cells can be readily manipulated for both recombination cleavage and end resolution. However, unlike the rapid coding joint formation in s/ + cells that have the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs), the process for resolving coding ends in scid cells is slow and error prone, and also appears to be correlated with a reduction in the RAG1/2 expression. Apparently, this process is mediated by a DNA-PK-independent pathway. The fact that the activity of this pathway can be manipulated in vitro makes it possible to delineate the mechanisms in end opening, processing and joining. Therefore, these ts-Ab-MLV transformed scid cell lines offer a model to study the molecular nature as well as the regulation of the DNA-PK-independent pathway in coding end resolution.
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PMID:The scid recombination-inducible cell line: a model to study DNA-PK-independent V(D)J recombination. 1116 62

Infection by human immunodeficiency virus (HIV) is associated with an early immune dysfunction and progressive destruction of CD4+ T lymphocytes. This progressive disappearance of T cells leads to a lack of immune control of HIV replication and to the development of immune deficiency resulting in the increased occurrence of opportunistic infections associated with acquired immune deficiency syndrome (AIDS). The HIV-induced, premature destruction of lymphocytes is associated with the continuous production of HIV viral proteins that modulate apoptotic pathways. The viral proteins, such as Tat, Env, and Nef, are associated with chronic immune activation and the continuous induction of apoptotic factors. Viral protein expression predisposes lymphocytes, particularly CD4+ T cells, CD8+ T cells, and antigen-presenting cells, to evolve into effectors of apoptosis and as a result, to lead to the destruction of healthy, non-infected T cells. Tat and Nef, along with Vpu, can also protect HIV-infected cells from apoptosis by increasing anti-apoptotic proteins and down-regulating cell surface receptors recognized by immune system cells. This review will discuss the validity of the apoptosis hypothesis in HIV disease and the potential mechanism(s) that HIV proteins perform in the progressive T cell depletion observed in AIDS pathogenesis.
Leukemia 2001 Mar
PMID:Using death to one's advantage: HIV modulation of apoptosis. 1123 54

Severe primary immunodeficiencies (PID) are rare; their global incidence is comparable to that of childhood leukemia; they include more than 100 different entities. Clinical manifestations are: unusually severe or frequent infections or infections that do not respond to adequate treatment; an increased risk of certain malignancies; sometimes auto-immune manifestations. Delayed diagnosis and management of PID can lead to severe and irreversible complications or to death. PID can become manifest only in the adult; in common variable immune deficiency, the median age at diagnosis is between the 2nd and the 3rd decade of life. PID are often transmitted genetically; recent progresses in molecular biology have allowed more precise and earlier, including antenatal, diagnosis. Molecular treatment of 3 infants with a severe immunodeficiency has recently been achieved in April 2000. Those progresses were mostly based on the study of immunodeficiency databases. We present here the work of a Belgian group specialized in PID; meetings have started in June 1997. This group establishes guidelines for the diagnosis and treatment of PID, adapted to the local situation. The elaboration of a national register of PID is also underway; this has to provide all guaranties of anonymity to patients and families. Such a register already exists at the European level; it has provided the basis for new diagnostic and therapeutic possibilities. The inclusion of Belgian data in this register should allow essential progresses essential for our patients.
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PMID:[Immune deficiencies: diagnosis, management, some perspectives]. 1138 26

The ts1 murine leukemia virus produces an immunodeficiency state in mice that parallels human immunodeficiency virus (HIV) infection in humans. Other murine leukemia viruses, such as LP-BM5 used in the murine acquired immune deficiency virus (MAIDS) model, have been studied extensively as a small animal model for HIV research, but lack many key similarities to HIV. Mice infected with ts1, however, utilize CD4 target cells for infection, undergo neuronal loss and demyelination, and develop clinical immunodeficiency. These features make this retrovirus in many ways an ideal candidate for a small animal model for HIV research. In this review article, the early development, the molecular and clinical pathogenesis of both the ts1 mutant of the Moloney murine leukemia virus and LP-BM5 are examined. Based on an extensive evaluation of the literature on LP-BM5 and ts1, it is concluded that the ts1 virus may serve as a better animal model to human retrovirus infection.
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PMID:Tsl and LP-BM5: a comparison of two murine retrovirus models for HIV. 1139 15

Seroepidemiological studies have shown previously that cancer patients are less likely to have antibodies against the tumour suppressive adeno-associated virus (AAV) than control groups. To examine the influence of AAV infection on the development of adult T-cell leukaemia lymphoma (ATLL), an endemic disease in Southern Japan that is caused by infection with the human T-cell leukaemia virus type 1 (HTLV-I), the prevalence of serum antibodies to AAV type 2 (AAV-2) was tested in healthy HTLV-I carriers (n = 39) and patients with ATLL (n = 31). The results showed a significant difference in AAV-2 seropositivity between the two groups: Only 29% of the ATLL patients had IgG antibodies against AAV-2, whereas 84.6% of the healthy HTLV-I carriers were seropositive. Analysis of total serum IgG and antibodies against the Epstein-Barr virus (EBV) EBNA1 antigen showed that the lack of AAV antibodies in patients was not due to an ATLL-associated immune deficiency. The lower level of AAV-2 seropositivity in ATLL-patients may indicate that AAV-2 antibody-positive HTLV-I carriers might be less likely to develop ATLL or that loss of AAV-2 antibodies may parallel the development of disease.
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PMID:Reduced prevalence of serum antibodies against adeno-associated virus type 2 in patients with adult T-cell leukaemia lymphoma. 1150 62


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